Evidence map›Paper›PMID 25481271›Full record

ReviewExperimental gerontology2015

How longevity research can lead to therapies for Alzheimer's disease: The rapamycin story.

Arlan Richardson, Veronica Galvan, Ai-Ling Lin, Salvatore Oddo

Open access · hybridAbstract readReview
In one paragraph

Review in Experimental gerontology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed
4.6field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

74 citing papers in PubMed, 122 citations in OpenAlex.

  1. Trial
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  8. mTOR inhibition enhances synaptic and mitochondrial function in Alzheimer's disease in an APOE genotype-dependent manner.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2024
    Article
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  18. Autophagy and apoptosis cascade: which is more prominent in neuronal death?Cellular and molecular life sciences : CMLS · 2021
    Review
  19. Article
  20. Review

14 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 4 institutions in 1 country.

Arlan RichardsonDepartment of Geriatric Medicine, University of Oklahoma Health Sciences Center, Oklahoma City VA Medical Center, Oklahoma City, OK 73104, USA. Electronic address: Arlan-richardson@ouhsc.edu.
Veronica GalvanDepartment of Physiology and Barshop Institute, University of Texas Health Science Center at San Antonio, San Antonio, TX 78245, USA.
Ai-Ling LinSanders-Brown Center on Aging, Department of Pharmacology & Nutritional Sciences, University of Kentucky, Lexington, KY 40536, USA.
Salvatore OddoBanner Sun Health Research Institute, Sun City, AZ 85351, USA; Department of Basic Medical Sciences, University of Arizona College of Medicine-Phoenix, Phoenix, AZ 85004, USA.
Banner Sun Health Research Institute · USThe University of Texas Health Science Center at San Antonio · USUniversity of Kentucky · USUniversity of Oklahoma Health Sciences Center · US

Funding

TRANSGENIC COREP30AG013319 · NIA · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI JAMES FLOYD NELSON · 1995 to 2026
$30.6M
Can Rapamycin Retard Age-Related Diseases?RC2AG036613 · NIA · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI RICHARDSON, ARLAN G. · 2009 to 2010
$5.2M
Molecular interplay between Abeta, tau and mTOR: Mechanisms of neurodegenerationR01AG037637 · NIA · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI ODDO, SALVATORE · 2011 to 2015
$1.6M
Neuroimaging Assessments of Brain Integrity in Aging MiceK01AG040164 · NIA · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI LIN, AI-LING · 2012 to 2016
$462k
Pathogenic Tau Promotes Brain Vascular Dysfunction in Alzheimer's DiseaseI01BX002211 · VA · SOUTH TEXAS VETERANS HEALTH CARE SYSTEM · PI GALVAN, VERONICA · 2015 to 2025
–
BLRD VA I01 BX002211NIA NIH HHS K01 AG040164NIA NIH HHS P30 AG013319NIA NIH HHS R01 AG037637NIA NIH HHS RC2 AG036613NIA NIH HHS RC2AG036613
6 · The paper itself

Abstract

The discovery that rapamycin increases lifespan in mice and restores/delays many aging phenotypes has led to the speculation that rapamycin has 'anti-aging' properties. The major question discussed in this review is whether a manipulation that has anti-aging properties can alter the onset and/or progression of Alzheimer's disease, a disease in which age is the major risk factor. Rapamycin has been shown to prevent (and possibly restore in some cases) the deficit in memory observed in the mouse model of Alzheimer's disease (AD-Tg) as well as reduce Aβ and tau aggregation, restore cerebral blood flow and vascularization, and reduce microglia activation. All of these parameters are widely recognized as symptoms central to the development of AD. Furthermore, rapamycin has also been shown to improve memory and reduce anxiety and depression in several other mouse models that show cognitive deficits as well as in 'normal' mice. The current research shows the feasibility of using pharmacological agents that increase lifespan, such as those identified by the National Institute on Aging Intervention Testing Program, to treat Alzheimer's disease.

Indexed as

Alzheimer DiseaseAnimalsAutophagyBehavior, AnimalCerebrovascular CirculationCognition DisordersDisease Models, AnimalLongevityMemory DisordersMiceNeurofibrillary TanglesPlaque, AmyloidSirolimusTOR Serine-Threonine KinasesVasodilator AgentsmTOR protein, mouseSirolimusTOR Serine-Threonine KinasesVasodilator AgentsAlzheimer's diseaseBehaviorCognitionRapamycin

Identifiers

PMID25481271
PMCPMC6417920
OpenAlexW2012904348

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.